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Role of Iron in Children With Immunoglobulin A Nephropathy and Macrohematuria-Induced Acute Kidney Injury
Shingo Ishimori1, Tomoko Horinouchi2, Tomohiko Yamamura2
1Department of Pediatrics, Takatsuki General Hospital, Takatsuki, Japan.
Insights
Pediatric IgA nephropathy with macrohematuria-induced acute kidney injury shows significant iron deposition in tubules. These children exhibit a good renal prognosis, with no decrease in kidney function observed.
Area of Science:
- Nephrology
- Pediatric Nephrology
- Immunopathology
Background:
- Pediatric Immunoglobulin A nephropathy (IgAN) with macrohematuria (MH)-induced acute kidney injury (AKI) is not well understood.
- Adults with MH-AKI often progress to chronic kidney disease, highlighting the need to study pediatric cases.
Purpose of the Study:
- To investigate the role of iron deposition and macrophage markers in pediatric IgAN with MH-AKI.
- To evaluate the renal prognosis of pediatric patients with MH-AKI IgAN.
Main Methods:
- Renal biopsy samples from pediatric patients with IgAN (with and without MH/AKI) and controls were analyzed.
- Immunohistochemistry was used to detect iron (Berlin Blue), CD163, and CD68.
- Clinical data were correlated with histopathological findings.
Main Results:
- Significant iron deposition (Berlin Blue staining) was observed in the injured tubulointerstitium of children with MH-AKI IgAN and MH(+)AKI(-) IgAN.
- CD163-positive cells were found near iron deposits, suggesting a role in hemoglobin scavenging.
- No children with MH-AKI IgAN experienced a decline in renal function during follow-up.
Conclusions:
- Children with IgAN and MH, with or without AKI, exhibit substantial iron deposition in renal tubules.
- CD163-positive cells may be involved in hemoglobin scavenging in MH-AKI IgAN.
- The renal prognosis for pediatric MH-AKI IgAN is favorable.
Introduction:
The role of iron in, and the prognosis of, pediatric Immunoglobulin A nephropathy (IgAN) with macrohematuria (MH)-induced acute kidney injury (AKI) (MH-AKI) have not been evaluated. Thirty percent of adults with MH-AKI, and especially those who are older, show progression to chronic kidney disease.
Methods:
We evaluated the immunohistopathologic characteristics of renal biopsy samples from pediatric patients with MH-AKI IgAN and controls, using Berlin Blue to identify iron, CD163 (a hemoglobin-scavenging receptor), and CD68 (a total macrophage marker), then compared the findings against the clinical characteristics of the patients.
Results:
We enrolled 44 children as follows: 19 with IgAN but no MH or AKI; 5 with IgAN and MH but no AKI (MH(+)AKI(-) IgAN); 11 with MH-AKI IgAN; and 9 with no IgAN, MH, or AKI, according to a renal biopsy. Berlin Blue staining was detected predominantly at the injured tubulointerstitium, and the areas of staining in children with MH(+)AKI(-) and MH-AKI IgAN were significantly more extensive. The areas of Berlin Blue and CD163 staining did not perfectly match; however, areas of Berlin Blue were surrounded by immunopositivity for CD163. No children with MH-AKI IgAN showed decreased renal function at their last visit.
Conclusion:
Children with IgAN and MH, with or without AKI, showed considerable iron deposition in their renal tubules. CD163-positive cells might scavenge hemoglobin in patients with MH-AKI IgAN, but not their roles as macrophages. The renal prognosis of pediatric MH-AKI IgAN is good.
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